Term
| What is the difference between myocardial infarction and myocardial ischemia? |
|
Definition
| Ischemia results from when O2 supply does not meet demand, whereas MI is necrosis caused by prolonged ischemia; therefore, you can have ischemia and not necessarily infarction. |
|
|
Term
| The inadequate coronary flow that causes ischemia/infarction is due to which- increased demand (exercise) or reduced supply of blood (occluded artery)? |
|
Definition
| Both, conversely the way to manage ischemia is to reduce demand or increase supply |
|
|
Term
| In the sequence of functional failure during MI, which of these two groups occurs first: 1- impaired rate of relaxation, impaired force generation, rapid K leak and Na gain, or 2- onset of contracture, onset of Na-K pump failure? |
|
Definition
| Group 1 occurs immediately, group 2 occurs after 15 minutes. |
|
|
Term
| What are the two metabolic responses to ischemia? |
|
Definition
| Huge increase in use of stored glycogen (anaerobic glycolysis), and sacrifice of creatine phosphate |
|
|
Term
| What are the 2 major causes of impaired heart muscle relaxation in MI, that is both related to reduced ATP and increased ADP concentration? |
|
Definition
| Reduced Ca resequestration by the SR, and increased ADP/ATP inhibits cross-bridge release |
|
|
Term
| True or False: During ischemia, LVEDV will be greater and the LVEDP will be lower. |
|
Definition
| False, LVEDV will be smaller due to reduced ability to relax and therefore LVEDP will be higher |
|
|
Term
| Which of the following happens early in ischemia to impair active force development - the garden hose effect, increased H+ and Pi inhibiting Ca binding to troponin, or increased ATP-sensitive K current which shortens systole. |
|
Definition
|
|
Term
| Since you decreased contractility during ischemia, what happens to stroke volume, LVEDP, LVEDV? |
|
Definition
| SV goes down, LVEDV increases because of leftover blood not ejected, LVEDP increases due to larger volume of blood and less relaxation |
|
|
Term
| True or False: the result of decreased ATP and increased ADP in the cell on the flux of K+ results in the opening of ATP sensitive K+ channels and opening of non-selective cation channels allowing Na+ to flow in the cell. |
|
Definition
| True, this shortens the action potential duration, and depolarizes the membrane and may cause arrythmias because Na channels become inactivated |
|
|
Term
| What is the result of intracellular Na rising in the cell during ischemia? |
|
Definition
| Membrane depolarization and an increase in intracellular Ca due to the NHE and Na/Ca exchangers. |
|
|
Term
| True or False: the fall in Ca levels in the cell results in activation of proteases, destruction of enzymes and cytoskeletal elements, intake of Ca in mitochondria resulting in functional arrest, depletion of high energy phosphates due to energy dependent Ca pump in mitochondria. |
|
Definition
| False, the rise Ca levels results in these things. |
|
|
Term
| When does necrosis occur in ischemia? |
|
Definition
| 20-30 minutes after onset, 3-6 hours after completed infarct |
|
|
Term
| Where in the vessel wall does necrosis start and end in infarction? |
|
Definition
| It starts in the subendocardium and moves to the epicardium |
|
|
Term
| Which of these are the major clinical findings of MI: angina, dyspnea, diaphoresis, nausea, bowel movements. |
|
Definition
| All except bowel movements. |
|
|
Term
| Which 3 enzymes can you check for in the blood due to MI (tissue necrosis)? |
|
Definition
| Troponin I and T, Creatine Kinase, Myoglobin |
|
|
Term
| What will you see in an ECG that reveals an MI? |
|
Definition
| ST interval elevation, for ischemia there is ST interval dperession |
|
|
Term
| In the management of ischemia how do you increase supply and reduce demand? |
|
Definition
| Increase supply by angioplasty, platelet inhibitors like aspirin/clopidigrel, thrombolytics, and bypass surgery; reduce MvO2 demand with beta blockers, reduce preload with nitrates (venodilators), ACE inhibitors like captopril due reduce afterload (vasodilation). |
|
|
Term
| What is the result of ischemia on coronary perfusion pressure? |
|
Definition
| The reduced diastolyic aortic pressure (less stroke volume) and increased diastolyic ventricular pressure (heart can’t relax) causes a reduction in perfusion pressure. |
|
|
Term
| What are the elements and steps of the Users Guide Method? |
|
Definition
| Begin with a clinical scenario (either PBL or real patient), Search online for published info, Select one or more studies, Read and critically appraise the studies (PICO, validity, results, application) |
|
|
Term
| In regards to UGM, what is PICO? |
|
Definition
| The criteria with which to frame searchable clinical questions - Patients, Intervention, Comparison Group, Outcome |
|
|
Term
| What are the equations for - relative risk, relative risk reduction, absolute risk reduction, and number needed to treat? |
|
Definition
| RR - treatment risk/control risk; RRR - control - treatment/control; ARR - control-treatment; NNT - 1/ARR |
|
|
Term
| What type of study is the gold standard for judging the impact of therapies? |
|
Definition
| Clinical trials, which should be performed when there is significant observational data but have important unanswered questions. |
|
|
Term
| In regards to studying therapies, what is a cointervention? |
|
Definition
| Interventions other than treatment under study that may be differentially applied to experimental and control groups, potentially biasing study |
|
|
Term
| What is irreversible perfusion injury? |
|
Definition
| A form of necrosis that does not occur until reperfusion of ischemic tissues, the longer it takes to reperfuse, the more likely that injury will occur |
|
|
Term
| Why does reperfusion of ischemic tissue cause damage, shouldn’t blood flow restore function? |
|
Definition
| Blood flow causes oxidative burst generating free radicals primarily from leukocytes but also endothelium and myocytes |
|
|
Term
| In reperfused ischemic tissues what happens after free radicals arrest metabolism? |
|
Definition
| They inhibit Na/K pump raising intracellular Na, stimulate Na/Ca exchanger (1Ca for 3 Na), leads to intracellular Ca overload, havoc ensues |
|
|
Term
| True or False: free radicals cause direct lipid peroxidation disrupting sarcolemma and also induce apoptosis (along with cytokines, neurotrans, Ca) |
|
Definition
|
|
Term
| In reperfused myocardium, what is stunning? |
|
Definition
| Reversible reperfusion injury, a key feature of which is to overcome contractility deficits with ionotropes. |
|
|
Term
| In reperfusion stunning, what is the relationship between Ca and force production? |
|
Definition
| Ca overload activates proteases, damaging myofilaments so that they are unable to respond normally to activation by Ca, decreases maximum force production |
|
|
Term
| What 2 things does an ACE inhibitor do? |
|
Definition
| Dilates vasculature and improves myofilament Ca response (good to treat stunning) |
|
|
Term
| What is Hibernating myocardium? |
|
Definition
| Chronically ischemic but not necrotic tissue with impaired contractility and relaxation, normal metabolism, akinetic or hypokinetic |
|
|
Term
| True or False: the best treatment for hibernating myocardium is ionotropic agents to improve function as opposed to revascularization. |
|
Definition
| False, ionotropes may provoke ischemia, revascularization is curative through angioplasty |
|
|
Term
| True or False: maladaptive remodeling, following myocardial necrosis, leads to ventricular reduction, decreased wall tension, and increasing function. |
|
Definition
| False, ventricular enlargement, increased wall tension, and deteriorating function. |
|
|
Term
| What 3 things do you use to prevent maladaptive remodeling? |
|
Definition
| B-blockers, ACE inhibitors, aldosterone antagonists |
|
|
Term
| Preconditioning of the heart is from repetitive bouts of brief ischemia, what is the benefit of this? |
|
Definition
| It confers protection against a more prolonged episode of ischemia and reperfusion, due to effectors like ATP-sensitive K+ channel |
|
|
Term
| In reperfusion injury, why is it advisable to only use ionotropes when absolutely necessary to prevent hypotension? |
|
Definition
| These agents increase MvO2, generating free radicals and giving less time for repair |
|
|
Term
| What is aortic stenosis and what is the ventricular response? |
|
Definition
| Degenerative and calcification change in valve reducing aortic valve area; the ventricle responds by concentric left ventriclular hypertrophy to normalize wall tension |
|
|
Term
| What is the symptomatic triad of aortic stenosis? |
|
Definition
| Dyspnea(diastolyic dysfunction increases fillng pressure backing up fluid in chest), angina (pain due to MvO2 supply/demand mismatch due to hypertrophy), vasodepressor syncope (too much dilation) |
|
|
Term
| In aortic stenosis, how does the modified myocardial perfusion gradient change heart blood supply? |
|
Definition
| The hypertrophied heart compresses coronaries resulting in decreased perfusion, in combo with decreased diastolyic aortic pressure reduces the hearts blood supply. |
|
|
Term
| What is the leading cause of mitral stenosis? |
|
Definition
|
|
Term
| What is the result of mitral stenosis in the short term and long term? |
|
Definition
| The obstructed blood flow causes an enlargement in the left atrium due to increased filling pressure; overtime, this often leads to development of atrial fibrillation (depriving patient extra 25% they would have in normal rhythym) and fixed pulmonary hypertension and right ventricular failure. |
|
|
Term
| During development, during which weeks does the cardiovascular system begin to develop and which week does it start to beat? |
|
Definition
|
|
Term
| During cardiovascular development, during which weeks does septation of the heart into four chambers happen? |
|
Definition
|
|
Term
| True or False: congenital heart defect are uncommon at <1% of births. |
|
Definition
| False, they are considered common, particularly cardiac/ventricular septal defects |
|
|
Term
| Failure of appropriate circulatory changes to occur at birth is the cause of two of the most common congenital anomalies, which are? |
|
Definition
| Patent oval foramen and patent ductus arteriosus |
|
|
Term
| During cardiovascular development, what is coarctation? |
|
Definition
| Descending aorta pinches off and fuses with patent ductus arteriosus or blood is shunted to collateral arteries |
|
|
Term
| What are the 5 T’s of cyanotic heart disease? |
|
Definition
| Truncus arteriosus (no aortic pulmonary septation), transposition of great arteries, tricuspid atresia, teratology of fallot, total anomalous pulmonary venous return |
|
|
Term
| In the teratology of Fallot, what does the acronym PROV stand for? |
|
Definition
| Pulmonary artery stenosis, right ventricular hypertrophy, over-riding aorta, ventricular septal defect |
|
|
Term
| What is aortic regurgitation and what are its symptoms? |
|
Definition
| It is the backflow of blood across the valve during diastole due to either intrinsic valve abnormalities or aortic root abnormalities; this problem presents with dyspnea and angina, with mid-diastolic crescendo murmur. |
|
|
Term
| What is the acute and chronic result of aortic regurgitation? |
|
Definition
| The acute response is mild increase in EF, increased LVEDP then pulmonary pressures and dyspnea; the chronic response is elevated EF, normalized LVEDP and eccentric hypertrophy of the heart, although there is a decompensation point where LVEDP rises, EF drops, and symptoms develop. |
|
|
Term
| What is the first abnormality that occurs in myocardial ischemia? |
|
Definition
|
|
Term
| What does an elevated or depressed ST segment indicate? |
|
Definition
| MI or Coronary artery disease |
|
|
Term
| What is the difference between S3 and S4 heart sounds? |
|
Definition
| S3 occurs after S2 and indicates blood flowing against a non-compliant ventricle in mid-diastole, S4 occurs before S1 at the end of diastole for the same reason |
|
|
